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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate a pediatric trace element supplement (Ped-El, Pharmacia) 18 metabolic balance studies were completed in 13 infants (mean birth weight 909 +/- 67 g, x +/- SEM; mean gestational age 27.2 +/- 1 weeks) who received total parenteral nutrition. The supplement supplied 40 micrograms/kg/day of zinc resulting in negative retention of 226 micrograms/kg/day. Copper infused at 20 micrograms/kg/day led to a positive retention of 8 micrograms/kg/day and an increase in serum Cu (p less than 0.05) not related to Cu intakes. Manganese infused at 40 micrograms/kg/day was nearly all retained (88 +/- 16% retention). Iron infused at 120 micrograms/kg/day led to a positive retention of 93 micrograms/kg/day. Although plasma ferritin and percent transferrin saturation were elevated, only plasma Fe values were correlated with Fe intake. This trace element supplement does not appear suitable for very low birth weight preterm infants.
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PMID:Zinc, copper, manganese, and iron balance of parenterally fed very low birth weight preterm infants receiving a trace element supplement. 313 48

We measured the serum selenium concentration in 64 patients with uncomplicated viral (n = 33) or bacterial (n = 31) infections during the acute state of infection, during the early convalescent phase and after a minimum recovery period of three weeks and compared it to serum iron values. Both selenium (mean +/- SEM: 70.3 +/- 2.3 micrograms/l vs 79.4 +/- 2.2 micrograms/l, p less than 0.0001) and iron (8.4 +/- 0.8 micrograms vs 16.7 +/- 0.9 micrograms/l, p less than 0.0001) concentrations showed significant depressions in the acute stage of infection compared with the values after the recovery. The reduction of serum selenium did not correlate with the severity of infection measured by fever. We conclude that acute infections decrease serum levels regardless of the infective agent. The changes are of interest because of the possible connection between selenium and the immune system.
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PMID:Serum selenium in acute infections. 318 86

The magnesium content of mononuclear blood cells (MBCs) may be a better indicator of intracellular or total body Mg status than either serum or red blood cell Mg. However, MBCs are a heterogeneous population composed primarily of lymphocytes and monocytes. A significant difference in the Mg concentration or content between lymphocytes and monocytes could alter the results for MBC Mg. We produced monocyte-poor MBCs (MPMBCs) by treating MBCs with carbonyl iron particles. We purified T lymphocytes from MPMBCs [antihuman F(ab)2 monolayer procedure]. The purity of T lymphocytes (T + NK cells) was 98% by flow-cytometric analysis. The mean (+/- SEM) Mg content and concentration of MPMBCs were 61.9 +/- 3.0 fg/cell and 10.6 +/- 0.4 mmol/l, respectively, and of T lymphocytes 60.8 +/- 2.7 fg/cell and 11.8 +/- 0.4 mmol/l, respectively. There was no significant difference in Mg content between MPMBCs and T lymphocytes. The Mg concentration of T lymphocytes was significantly higher (p less than 0.001) than MPMBCs. However, the difference is small and does not justify the increased complexity of the assay for T lymphocytes. We conclude that the cell composition of MBCs may affect the result for Mg concentration.
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PMID:Magnesium content and concentration of mononuclear and T lymphocyte blood cells. 326 48

An increased incidence of diabetes mellitus and glucose intolerance has been reported in thalassaemia major treated with a high transfusion programme (HTP). To investigate beta-cell function, serum immunoreactive insulin (IRI), C-peptide (CP) and glucose were measured fasting and at 3, 6 and 10 min after i.v. administration of 1 mg glucagon in 20 thalassaemia patients treated by many transfusions and in nine healthy control subjects. Fasting C-peptide concentrations (mean +/- SEM) were higher in the thalassaemic group (2.15 +/- 0.17 ng/ml) than in the controls (1.41 +/- 0.13 ng/ml). After stimulation with glucagon, C-peptide concentrations were consistently higher (P less than 0.01) by approximately 50% in the thalassaemic than in the control group (5.29 +/- 0.31 vs 3.36 +/- 0.21 ng/ml, at 3 min; 5.22 +/- 0.30 vs 3.53 +/- 0.21 ng/ml at 6 min and 4.69 +/- 0.27 vs 3.30 +/- 0.17 ng/ml after 10 min). Plasma IRI concentrations increased in both groups after glucagon stimulation but were not significantly different. The glucose values were approximately 15% higher at each sampling time in the thalassaemic group than those of the normal subjects. It is concluded that disturbances in carbohydrate metabolism in thalassaemia major treated with HTP are the consequence of hepatic cirrhosis which accompanies secondary haemosiderosis, and possibly iron deposition in the beta-cells of the pancreas.
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PMID:A study of beta-cell function after glucagon stimulation in thalassaemia major treated by high transfusion programme. 332 97

We have examined the effect on iron stores of blood transfusions given to premature neonates during hospitalization in the neonatal intensive care unit as reflected by serum ferritin levels measured for 6 months after discharge. Premature infants who were transfused with more than 100 ml packed cells (group D; n = 11) had higher ferritin levels for a longer period than premature infants who were transfused with smaller volumes (group c; n = 9) or premature and mature infants who were not transfused at all (group B; n = 24 and group A; n = 21, respectively). At 4-5 months the serum ferritin levels in group D (489.8 +/- 132.1 micrograms/L; mean +/- SEM) were significantly higher (P less than 0.001) than those of the other groups. The level of group A term infants (77.5 +/- 12.5 micrograms/L) was higher than those of group B premature infants who did not receive a blood transfusion (33.0 +/- 7.1 micrograms/L) or group C who received less than 100 ml (36.5 +/- 8.8 micrograms/L packed red blood cells. However, these differences were not statistically significant. Our data demonstrate that very-low-birthweight infants who receive a large volume of packed cells during hospitalization may accumulate iron stores sufficient for red cell production during the first 6 months of life. Administration of large amounts of supplemental iron, in such cases, may be curtailed.
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PMID:Serum ferritin levels in preterm infants after multiple blood transfusions. 333 57

Previous investigations have shown that alveolar macrophages from cigarette smokers contain more iron than do macrophages obtained from nonsmokers. To localize intracellular iron and to help assess its potential for participation in the production of hydroxyl radicals, macrophages were fractionated and the ferritin and iron contents were measured in various cell fractions. Alveolar macrophages from seven smokers and six nonsmokers were lysed by nitrogen cavitation and centrifuged, first at 500 g and then at 11,000 g. Measured by radio-immunoassay, the total cellular ferritin was 133.8 +/- 33.2 ng and 782.0 +/- 177.8 ng per 1 x 10(6) macrophages (mean +/- SEM, p less than 0.01) obtained from nonsmokers and smokers, respectively. The total cellular iron contents were 7.5 +/- 0.6 nmol and 27.6 +/- 4.8 nmol per 1 x 10(6) macrophages (p less than 0.02) obtained from nonsmokers and smokers, respectively. The accumulation of iron by smokers' alveolar macrophages correlated with the number of cigarettes that had been smoked. Forty-two percent of the iron but only 9% of the ferritin was contained in the pellet obtained from centrifugation at 500 g. The pellet from the second centrifugation contained approximately 33% of the iron and 5% of the ferritin. The supernatant resulting from the second centrifugation contained 25% of the iron and 85% of the ferritin. Cigarette smoking did not appear to alter the intracellular distribution of either iron or ferritin. The ferritin content of bronchoalveolar lavage fluid was 0.10 +/- 0.04 micrograms/mg and 0.90 +/- 0.18 micrograms/mg albumin for nonsmokers and smokers, respectively (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Iron and ferritin contents and distribution in human alveolar macrophages. 337 7

To investigate whether iron is involved in the reperfusion syndrome by aggravating free radical injury, the hearts from iron-loaded and control rats were perfused under normoxic, anoxic, and reperfusion conditions. Normoxic perfusion revealed no change in coronary flow, contractility, or lactate dehydrogenase (LDH) release between these two groups. Under anoxic and reperfusion conditions, however, we found a significant increase of ventricle fibrillation (56% vs. 0%, p less than 0.01, n = 9), a significantly lower recovery of contractility (21 +/- 7.4% vs. 81 +/- 6.6%, mean +/- SEM; p less than 0.001), and a significant increase of LDH release (667 +/- 142 vs. 268 +/- 37 mU LDH/min/g wet wt, mean +/- SEM; p less than 0.05). Administration of either 20 microM of the antioxidant (+)-cyanidanol-3 or 50 microM of the iron-chelator deferoxamine totally prevented the generation of ventricle fibrillation and normalized contractility to control levels in the iron-loaded group. Moreover, 20 microM (+)-cyanidanol-3 significantly lowered LDH release in this period (312 +/- 67 mU), whereas deferoxamine had no protective effect on this LDH release (1,494 +/- 288 mU). Normal hearts appeared to be protected by 20 microM (+)-cyanidanol-3 as well. In this group (n = 6), a significantly higher recovery of contractility (97.1 +/- 3.2% vs. 81 +/- 6.6%, p less than 0.05) and a significantly lower release of LDH (110 +/- 27 vs. 268 +/- 37 mU, p less than 0.05) was found compared with the control group (n = 9). No difference in superoxide dismutase or glutathione peroxidase activity was found between the groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Iron-load increases the susceptibility of rat hearts to oxygen reperfusion damage. Protection by the antioxidant (+)-cyanidanol-3 and deferoxamine. 339 80

Activated macrophages inhibit replication of murine lymphoblastic leukemia L1210 cells without lysis. This inhibition of replication is associated with abnormalities of mitochondrial electron transport at the level of NADH dehydrogenase (NADH-DH) and succinate dehydrogenase (SDH). The mechanism of inhibition is unknown, although it has been demonstrated that as NADH-DH and SDH activity is lost, iron is released from cells. Because both NADH-DH and SDH contain numerous iron-sulfur clusters, damage to these structures may be one result of injury by activated macrophages. L1210 cells were labeled with 55Fe and co-cultivated with activated murine peritoneal macrophages (injured L1210 cells). At 48 h, injured L1210 cells had released 83 +/- 8% (mean +/- SEM of 55Fe activity into the media, compared with 25 +/- 4% release from control and 37 +/- 7% from nondividing mitomycin C-treated control cells. All cells were greater than 90% viable. These differences were also reflected in the iron content of the cells. Mitochondria were then separated by centrifugation after cell disruption and 55Fe activity was found to be similarly decreased in both mitochondrial and nonmitochondrial fractions of injured L1210 cells. To further characterize the changes in mitochondrial iron content, mitochondrial proteins from injured and control L1210 cells were separated by IEF and 55Fe activity of gel slices was determined. There was selective loss of 55Fe activity in the area of the gel corresponding to SDH and NADH-DH, suggesting that iron loss from iron-sulfur clusters may occur in L1210 cells injured by activated macrophages. Iron uptake into L1210 cells after removal from macrophages showed a rapid large influx of radioactive iron. L1210 cells in contact with macrophages appear to develop an iron-depleted state, which is dependent on the continued presence of macrophages.
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PMID:Mitochondrial iron loss from leukemia cells injured by macrophages. A possible mechanism for electron transport chain defects. 339 40

The brown pigmentation of the skin associated with venous ulceration is caused by increased local iron deposition. Diagnostic x-ray spectrometry, a method based on x-ray fluorescence analysis, was used for the noninvasive determination of iron levels in the skin of patients with venous ulceration. The mean (+/- SEM) iron concentration in the skin around the venous ulcer was elevated, compared with control values of nonulcerated skin (250 +/- 54 vs 128 +/- 39 micrograms) and compared with normal skin from the forearm (250 +/- 54 vs 14 +/- 2.5 micrograms). These data suggest that dermal iron deposition may not be an incidental by-product of increased venous pressure, but may actively perpetuate tissue damage in venous ulcerations.
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PMID:Overload of iron in the skin of patients with varicose ulcers. Possible contributing role of iron accumulation in progression of the disease. 341 80

Before 1971 the incidence of aseptic necrosis in renal transplant recipients was 29%, and after 1971 it was 5%. To investigate the reasons for this decreased incidence and to elucidate the causes of aseptic necrosis we studied all 26 transplant patients with aseptic necrosis and 42 controls matched for year of transplantation, age, and sex. Development of aseptic necrosis was not related to duration of dialysis before transplant, severity of uremia at the time the patient started dialysis, adequacy of dialysis before transplantation, transplant dysfunction at the time aseptic necrosis was diagnosed, hyperparathyroidism before or after transplantation, lack of Vitamin D supplementation after transplantation, or fatty infiltration of liver. Total steroid dose 1 month after transplantation was actually lower in aseptic necrosis compared with the control group (2.47 +/- 0.3 g vs. 3.6 +/- 0.3 g SEM g) and was similar after 4 months (6.72 +/- 0.55 g vs. 7.14 +/- 0.6 g), as were total numbers of i.v. doses of methylprednisolone or hydrocortisone. However, blood urea nitrogen (BUN) during the dialysis period was significantly higher in the aseptic necrosis group. Of the aseptic necrosis group, 27% had a previous transplant compared with 5% of controls. Half the aseptic necrosis group (5/10) had parenchymal iron on liver biopsy one year after transplant compared with 15% (2/13) of those without aseptic necrosis. Patients transplanted before 1971 (with and without aseptic necrosis) received significantly more i.v. hydrocortisone and less i.v. methylprednisolone, had higher BUN levels at the time of starting dialysis, and had lower serum calcium and higher serum phosphate at transplantation compared with patients transplanted in or after 1971. The incidence of aseptic necrosis following transplantation has decreased during the past 13 years for reasons that are unclear. Risk factors for aseptic necrosis may include previous transplantation, severe iron overload that may lead to marrow fibrosis and osteopenia, and increased protein catabolism/turnover during dialysis.
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PMID:The decreased incidence of aseptic necrosis in renal transplant recipients--a case control study. 351 82


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